Single mutation in H5N1 bird flu virus may make it more infectious to humans, study finds
"A study published Thursday contains a sobering piece of news about the H5N1 bird flu viruses circulating in cows in the United States: A single mutation in the hemagglutinin, the main protein on H5N1’s exterior, could turn a virus that is currently not well equipped to infect people into one that is much more capable of doing so.
"Scientists from Scripps Research, in La Jolla, Calif., reported in the journal Science that one mutation in the hemagglutinin changed the type of cell receptors that the virus is best suited to attach to, switching its preference from those found in birds to those that abound in the human upper respiratory tract"The authors termed their finding “a clear concern” — a view shared by other influenza scientists asked to review the paper by STAT. Debby van Riel, a virologist at Erasmus Medical Center in Rotterdam, the Netherlands, suggested it could be that the version of the virus currently spreading in cows has a higher zoonotic potential — a greater capacity to jump species — than previous iterations of H5N1. But she and others, including the Scripps team themselves, cautioned that this one change on its own might not be enough to morph this virus into an efficient human pathogen.
"While “the mutation to recognize human-type receptors is a crucial step, additional mutations are likely required for the virus to become fully transmissible between humans,” Yoshihiro Kawaoka, a flu virologist cross-appointed to the University of Wisconsin-Madison and the University of Tokyo, told STAT in an email. “Unfortunately, we don’t yet know what these additional mutations might be, as this area of research has not been extensively studied.”
"Adding to the concern the findings are provoking is the fact that a mutation at the same position on the hemagglutinin that the group studied was recently seen in viruses taken from a teenager in British Columbia, Canada, who contracted H5N1 around the end of October and became seriously ill. The teenager has been in critical condition in a Vancouver hospital for several weeks. Authorities there have been unable to determine how the teen became infected.
"The mutation in the Canadian teenager was at a position known as 226 on the hemagglutinin’s receptor binding site — the one the Scripps team found was critical to switching the receptor binding preference. But the amino acid changes in the teen’s virus were not identical to the ones shown by the Scripps team to alter the receptor binding preference. The mutation at position 226 was one of two important changes in the hemagglutinin seen in the virus from the teenager.
"It’s not known if the mutation was in the virus that first infected the teenager, or if it developed in the teen during the course of the infection — though scientists suspect the latter. It appears, though, that the teenager — who is no longer infectious — did not pass the virus anyone else, so that mutated virus will have died out.
"Scott Hensley, a professor of microbiology at the University of Pennsylvania’s Perelman School of Medicine, described the finding that a single mutation could change the receptor binding preference of this version of H5N1 as “alarming” — especially in light of the Canadian case.
“I think there’s a chance — I’m not saying it would [have] happened, but I think there’s a chance that those two substitutions in that British Columbia case could have triggered a pandemic if there were enough people exposed to that virus,” Hensley said.
"It’s long been assumed that H5N1 or any bird flu virus would need to switch its receptor binding preference in order to gain the capacity to spread easily among people — a development that would trigger a pandemic. This type of binding switch was seen in the 1918, 1957, 1968, and 2009 flu pandemics. But work conducted by the Scripps team on earlier versions of H5N1 suggested multiple mutations would be needed to achieve this end.
"This time was different."
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